15. Cardiovascular and Renal Medications

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Cardiovascular and Renal Medications

Objectives

Key Terms

action potential duration (ĂK-shun PŌ-těn-chăl, p. 220)

congestive heart failure (CHF) (HĂRT FĀL-yŭr, p. 229)

chronotropic (KRŎ-nō-TRŌP-ĭk, p. 221)

compelling indications (p. 238)

dehydration (dē-hī-DRĀ-shŭn, p. 247)

depolarization (dē-pō-lăr-ĭ-ZĀ-shŭn, p. 221)

digitalis toxicity (dĭj-ĭ-TĂL-ĭs, p. 231)

digitalizing dose (DĭJ-ĭ-tăl-īz-ĭng, p. 231)

dromotropic (DRŎM-ō-TRŎP-ĭk, p. 221)

dysrhythmia (dĭs-RĬTH-mē-ă, p. 219)

ectopic beats (ěk-TŎP-ĭk, p. 220)

edema (ě-DĒ-mă, p. 229)

effective refractory period (rē-FRĂK-tŏr-ē, p. 220)

electrocardiogram (ECG) (ě-lěk-trō-KÄR-dē-ō-gram, p. 219)

end-organ damage (p. 238)

fluid and electrolyte mixtures (ě-LĚK-trō-līt, p. 247)

hyperlipidemia (hī-pěr-lĭp-ĭ-DĒ-mē-a, p. 224)

hyperlipoproteinemia (hī-pěr-līp-ō-PRŌT-ě-NĒ-mē-ă, p. 226)

myocardial infarction (MI) (mī-ō-KÄR-dē-ăl ĭn-FÄRK-shŭn, p. 225)

myocardium (mī-ō-KÄR-dē-ŭm, p. 219)

normal sinus rhythm (SĪ-nŭs RĬTH-ĭm, p. 219)

pacemaker (PĀS-MĀ-kěr, p. 219)

positive inotropic action (ĭ-nă-TRŎP-ĭk, p. 230)

primary hypertension (PRĪ-măr-ē hī-pěr-TĚN-shŭn, p. 233)

secondary hypertension (SĔK-ŏn-dār-ē hī-pěr-TĚN-shŭn, p. 233)

Overview

image  http://evolve.elsevier.com/Edmunds/LPN/

This chapter is divided into six major sections, each with a focus on an important job of the cardiovascular, circulatory, or renal system. Some cardiovascular drugs have more than one action and are used for several reasons in the patient with cardiovascular problems. However, they are usually classified into one of the major drug categories.

The first section, Antianginals and Peripheral Vasodilators, focuses on the drugs used to treat chest pain from angina and problems with diseases causing blockage of the arteries, mostly in the legs. These drugs are widely used, and the nurse will have a major role in teaching the patient how to properly store and use them. The second section discusses the four major classes of medications used for dysrhythmias (irregular heartbeats). The antidysrhythmics are powerful drugs, and there may be many adverse reactions from some of these medications. The third section looks at lipids (fats) and the problem of lipoprotein abnormalities. Antihyperlipidemic agents are discussed as a part of the overall therapy for lipoprotein problems. The fourth section focuses on the drugs that make the heartbeat stronger—the cardiotonics or positive inotropic agents, such as digitalis and related products. These are some of the most common drugs for patients both in and out of the hospital, and some of the “must know” drugs. Antihypertensives, diuretics, and urinary system drugs are explored in the fifth section. Because hypertension (high blood pressure) is so common, the nurse will use many of these drugs. The latest guidelines for lowering blood pressure are listed, as well as common adverse reactions to these drugs. Although most of the drugs acting on the kidney are diuretics, other agents that affect the urinary tract are also presented here. The sixth section covers fluid and electrolytes, which nurses also frequently give.

These classifications have many drugs and these sections give the most important basic information about each drug category. If the nurse reviews the anatomy and physiology of the cardiovascular and urinary systems at the same time, it will help them understand both the problems that occur in these systems and how the different drugs act to solve those problems.

Cardiovascular and Urinary Systems image

The cardiovascular system is made up of the heart, blood vessels (Figure 15-1), and blood. This system moves nutrients (substances that support life and growth), waste products, gases, and hormones through the body. It also plays a role in the immune response and changes in body temperature.

Using special cardiac muscle and nerve systems, electrical impulses tell the heart muscle when to contract, forcing blood from the heart, through blood vessels, and out through the body. Arteries move blood from the heart to tissues using smaller branches called arterioles. Veins move blood from tissues back toward the heart, beginning with their smaller branches, called venules. Capillaries are very small vessels that link arterioles and venules.

The heart is the pump of the circulation system. The heart itself is fed by small coronary arteries that send nutrients to it during the resting phase of the cardiac cycle. The heart may weaken with disease and age and become less efficient. Sometimes the arteries become stiff and the walls become filled with fatty plaques from cholesterol or lipids. This condition is called atherosclerosis. In patients with hypertension, the blood vessels become less elastic, and the increased pressure against which the heart has to pump causes the heart to work harder. Thus diseases or abnormal conditions of the heart, arteries, or veins produce more stress on the heart itself. When blood cannot flow through the heart muscles, the muscles hurt from lack of oxygen (angina). This severe chest pain is called angina pectoris. In a heart attack (myocardial infarction [MI]), some of the heart muscle cells actually die and a scar forms. Medicine can often control the pain of angina and prevent heart attacks when the heart doesn’t have to work so hard.

Many of the cardiovascular drugs also have either direct or indirect action on the urinary system (Figure 15-2). The kidneys, urinary bladder, and ducts that carry urine work together to remove waste products from the circulatory system, to regulate blood pH and ion levels, and to maintain water balance. Strong pumping of the heart, good circulation through the vessels, and the full removal of waste products through the urinary system are all needed to keep the body’s fluids and electrolytes in balance.

image
FIGURE 15-2 Urinary system.

Antianginals and Peripheral Vasodilators

Overview

Narrowing or constriction of the smooth muscle in the small coronary arteries of the heart and the peripheral vascular system (vessels in the arms and legs) reduces the amount of blood carried to the heart and the peripheral tissues (Figure 15-3). When there is a lack of blood supply to bring oxygen and nutrients to the heart or to peripheral tissues, the pain of angina or peripheral vascular disease is felt.

Action

The heart receives its blood supply and oxygen from the coronary arteries. These small arteries are often plugged or damaged when the patient has angina or a heart attack. Blood may also be cut off from the coronary arteries if there is coronary vasospasm. Blockage or spasm causes cardiac angina when the heart muscle is without oxygen. Currently there are three major classes of drugs used in the medical management of angina. Nitrates (both short and long acting), β-blockers, and calcium channel blockers. Some other vasodilating agents (agents to open up the vessels) are used for increasing circulation in peripheral vascular disease. (Information about the use of beta blockers in treating angina by decreasing the oxygen demands of the heart and calcium channel blockers that may relieve angina by dilating the coronary vessels and reducing the work load of the heart can be found in the discussion of antihypertensives and diuretics in the fifth section of this chapter.)

Nitrates

Nitrate products have a direct action on vascular smooth muscle and cause it to relax. This effect is felt in both the circulation in arteries and veins. Arterial relaxation reduces the pressures the heart has to pump against (afterload), whereas venous relaxation helps in pooling of venous blood, thereby decreasing the amount of blood returned to the heart (preload). These effects work together to decrease myocardial oxygen use. In addition, nitrates increase the use of the other small blood vessels in the heart (collaterals) so that there is better oxygen supply to the inner layers of the heart muscle.

Calcium Channel Blockers image

Calcium is an electrolyte that helps move electrical impulses through cardiac tissue. Calcium channel blockers are drugs that help slow down the flow of calcium ions across the cell membrane, thus reducing the amount of calcium available for electrical impulse movement. The drugs in this group are used for a variety of actions. Some calcium channel blockers act directly on vascular smooth muscle to dilate (open up) coronary arteries and arterioles, which relieves anginal pain because more oxygen can go to the cardiac tissue. Other calcium channel blockers are used to reduce the response of the cardiac conduction system to electrical impulses and treat cardiac dysrhythmias. They are also used along with other drugs to treat hypertension. (See the sections on anti­dysrhythmics and antihypertensives for additional information on calcium channel blockers and beta-adrenergic blockers.)

Peripheral Vasodilators

Patients with occlusive arterial disease (blockage of the arteries that makes them smaller) have been treated with vasodilating drugs (drugs that help expand or open up the arteries), but with only limited success. These patients have decreased blood flow, which produces cold extremities, thin shiny skin, decreased hair growth on the legs, and the inability to walk without experiencing pain in their legs. Vasodilator drugs relax the smooth muscles of peripheral arterial blood vessels and help lead to better circulation to the arms and legs (Figure 15-4).

Uses

Rapid-acting nitrates (such as amyl nitrite, sublingual nitroglycerin, and sublingual or chewable isosorbide dinitrate) are used mostly to relieve pain in acute angina. The long-acting nitrates and topical, transdermal, transmucosal, and oral sustained-release nitroglycerin products are used to prevent or treat anginal attacks when they are likely to occur (for example, with exercise) and to reduce the severity and frequency of anginal attacks. They are also used to reduce the work of the heart in cases of MI and in chronic heart failure; and for relief of gallbladder, gastrointestinal (GI), urethral, and bronchial smooth muscle pain.

It is not always clear if it is safe to use nitroglycerin in patients with acute MIs. When it is used in patients with recent MIs, the transdermal patch systems work best, but patients must be closely evaluated. Intravenous (IV) nitroglycerin is used to control severe angina in an acute MI and also to control acute pain during procedures on the heart, such as cardiac catheterization. This IV nitroglycerin requires careful monitoring of the patient in a cardiac care or critical care unit due to the possibility the medicine may cause a severe drop in blood pressure.

Peripheral vasodilating agents are used to treat pain in the legs caused by problems such as intermittent claudication, arteriosclerosis obliterans, Raynaud’s disease, nocturnal leg cramps, and vasospasm caused by blood clots.

Adverse Reactions

There are many common adverse reactions to nitrates, including flushing, postural hypotension (low blood pressure when a person suddenly stands up), tachycardia (rapid heartbeat), confusion, dizziness, fainting, headache, light-headedness, vertigo (feeling of dizziness or spinning), weakness, drug rash, localized pruritus (itching), local burning in the mouth, nausea, and vomiting.

Some of these cardiac preparations contain tartrazine, a chemical that may cause an allergic type of reaction with symptoms similar to asthma. Patients who are allergic to aspirin have a greater chance of reacting to tartrazine.

When nitrate products are used, high doses may cause violent headaches. All nitrates should be given with care to patients with a recent history of stroke or cerebrovascular accident, because these conditions cause widening of the cerebral arteries.

Peripheral vasodilating agents may cause dizziness, headache, weakness, tachycardia, flushing, postural hypotension, dysrhythmias, confusion, severe rash, nervousness, tingling, and sweating. Some side effects disappear within a few weeks if they are mild and if the patient can keep taking the medication.

image Clinical Goldmine

Tolerance to Nitrates

Tolerance to nitrates may develop over time with repeated use. If the patient develops tolerance to one nitrate, it is likely that tolerance to other nitrates (cross-tolerance) will develop. Alternative coronary vasodilators may have to be used.

Drug Interactions

Nitrates increase the effects of atropine-like drugs and tricyclic antidepressants and decrease the effects of all choline-like drugs. The action of anticholinergic drugs and antihistamines may be made stronger. Nitrates should not be taken at the same time as prazosin because of the possibility of a significant interaction. Taking alcohol, beta blockers, antihypertensives, narcotics, and vasodilators with nitrates and nitrites (especially amyl nitrite) may produce severe hypotension (low blood pressure) and cardiac collapse. Nitrates may antagonize (interfere with) the vasopressor actions of sympathomimetic drugs. A cold environment or the use of tobacco reduces the action of nitroglycerin.

The action of peripheral vasodilating agents is stronger if used with antihypertensives and alcohol and may cause hypotension.

imageNursing Implications and Patient Teaching

n Assessment

Learn as much as possible about the health history of the patient. Ask about heart disease, other health problems, the possibility of pregnancy, allergies, smoking, and whether the patient is taking other drugs that may cause interactions. Get a full description of the angina pain.

n Diagnosis

What other problems does this patient have that may interfere with treatment? For example, is the patient overweight? Does he or she smoke? What is the patient’s understanding of what is happening? What is the patient’s nutritional status and what dietary habits does the patient have? Is there any problem with the patient’s kidneys?

n Planning

Many times angina may be reduced or controlled if the patient makes lifestyle changes. This might include stopping smoking, limiting alcohol, limiting salt (sodium), increasing physical exercise, losing weight, eating a balanced diet rich in fruits and vegetables with lots of potassium and magnesium, avoiding dietary saturated fats, reducing stress, and treating other diseases such as hypertension and hyperlipidemia. Some patients who have the coronary arteries blocked may be candidates for surgery (coronary arterial bypass grafts or percutaneous transluminal coronary angioplasty) to reduce the symptoms. Medications are also an important part of treatment.

In reviewing the medicines that might be ordered, refer to the information in Table 15-1, which compares the action of various nitrate products. Nitrates are readily absorbed under the tongue, from nasal spray, through the skin, and orally, but products taken orally are rapidly changed in the liver to inactive products. The half-life for nitroglycerin given sublingually (under the tongue) is only 1 to 4 minutes. Newer forms of the medication can be applied directly to the skin or used as a patch, allowing nitrates to pass directly into the bloodstream, thus reaching the heart before being destroyed by the liver.

image Table 15-1

Comparison of Nitrate Products

PRODUCT ONSET DURATION PREPARATION
Agents for Acute Angina
Amyl nitrate (Vaporole) Short-acting 10-30 seconds; repeat 3-5 minutes   Inhalation
isosorbide dinitrate (Dilatrate SR, Isordil, Sorbitrate, Titradose) 2-3 min 1-2 hr Sublingual/chewable
May take 5-10 minutes before activities that may cause pain. Take every 5 minutes × 3 doses in 15 minutes for acute pain.
nitroglycerin image (Nitrostat, Nitro-Dur, NitroTime, Nitro-Bid, Nitrolingual pump spray) 1-3 min 3-5 min Sublingual
1-2 min 4-6 hr Transmucosal
Immediately 5-10 min Intravenous, translingual
Agents for Angina Prophylaxis
isosorbide dinitrate 45-60 min 8 hr Oral
Slow 12 hr Sustained release, PO
isosorbide mononitrate (Ismo, Imdur, Monoket) 45-60 min 6 hr Oral, sustained release
nitroglycerin image (Nitro-Time, Nitro-Bid, MiniTran, Nitro-Dur) 24-45 min 3-8 hr Sustained release, PO
30-60 min 3-7 hr Topical ointment
30-60 min 8-10 hr Transdermal Patch. Remove for 12 or 24 hr to reduce development of tolerance.
Ranolazine (Ranexa ER) Variable Variable Extended release product. Do not take with grapefruit.

Image

PO, By mouth.
image Indicates “Must-Know Drugs,” or the 35 drugs most prescribers use.

n Implementation

Review Chapter 10 for the ways to administer different types of nitroglycerin products.

Nitrate headaches often go away with a lower dose and analgesics. As the patient continues to take the nitroglycerin product, these headaches will gradually stop.

Table 15-2 provides a list of peripheral vasodilating medications.

image Table 15-2

Peripheral Vasodilating Medications

GENERIC NAME TRADE NAME USE MOST COMMON OR SERIOUS ADVERSE EFFECTS
hydralazine Apresoline Essential hypertension, CHF from high afterload Angina, tachycardia, peripheral neuritis, blood dyscrasias, constipation, paralytic ileus, nausea, vomiting, diarrhea

Image

CHF, Congestive heart failure.

n Evaluation

The drug should be stopped if blurred vision or dry mouth occurs. If the patient says that some of the sustained-release medication is being passed in the stool, it is likely that food moves through the patient’s GI tract too fast to allow the drug to be absorbed. Such patients may need to switch to transdermal or sublingual medication.

Older adult patients may have postural hypotension with these drugs and need to be watched very carefully. They may need to have someone with them when they take the medication.

The patient must learn the uses and limits of the nitrate being taken, understand the schedule of when to take the drug, and be given information about when to call for help if chest pain does not go away after taking the drug. There are many important things to learn about giving this medication by its various routes. A person who has been using a nitrate for a long time should not stop taking the drug suddenly as this may cause more angina.

image Clinical Pitfall

Anginal Attacks

For acute angina, the patient should put one tablet under the tongue as soon as the pain begins. The medication should not be chewed or swallowed; it should be left to dissolve under the tongue. The patient should lie down and rest. If the pain is not relieved within 3 to 5 minutes, a second pill may be taken. If the pain is not relieved within another 3 minutes, a third pill may be taken. If the pain is still not relieved, the patient should chew an aspirin to help reduce blood clotting and be taken to an emergency room immediately to be evaluated for acute MI.

image Clinical Pitfall

Patient History of Chronic Heart Failure

The antidysrhythmic drugs often cause or worsen chronic heart failure or urinary retention. Patients with a past history of heart failure should be watched carefully.

n Patient and Family Teaching

Tell the patient and family the following:

• Nitroglycerin is very fragile and chemically breaks down rapidly; sunlight speeds up this process. Even under the best conditions, these drugs lose their strength 3 months after the bottle has been opened. The patient will need a new prescription every 3 months, and any old drugs should be thrown away. There was a time when a burning feeling under the tongue could tell the patient if nitroglycerin medication was still good, but this is no longer true. Medication that is still active produces a throbbing headache. If the patient fails to feel the throbbing in the head, usually the medication has lost its potency (strength).

• The headache usually lasts no longer than 20 minutes and may be relieved with analgesics. The patient should rest for 10 to 15 minutes after the pain is relieved. The physician should be notified if blurred vision, persistent headache, or dry mouth occurs.

• The medication should be taken on an empty stomach when possible.

• The patient must not drink alcoholic beverages while taking nitrate products.

• The topical ointment tube should be kept tightly closed. Store nitroglycerin in the refrigerator.

• Patients using inhalant medication should take it only when lying or sitting down. Because this is a product that will catch fire easily, the patient must not smoke and should avoid using the drug around fire or sparks.

• The topical ointment should be spread in a thin layer on the skin, using an applicator and a ruler. The ointment should not be rubbed or massaged into the skin. The patient should wash off any medication that might have gotten on the hands.

• For transdermal application, the patient should select a hairless spot (or clip hair) and apply the adhesive pad to the skin. Washing, bathing, or swimming does not affect this system. If the pad does come off, it should be discarded and a new one placed on a different site.

• For patients who may have developed tolerance to the drug, stopping the drug for several days may be long enough to make the body sensitive to it again. The smallest possible dose should be taken to reduce the risk of tolerance. Some patients have been instructed to apply the patch in the morning and remove it at night. However, as the ability of the heart to provide circulation is often at its lowest point in the early morning hours, this is when many MI’s develop—so removing the patch is NOT a good idea.

• The patient should keep a record of every anginal attack, the number of pills taken, and any side effects. The patient should bring this record to each visit to the health care provider.

• The patient should use nitroglycerin when anginal attacks are likely; taking the medication before the activity may prevent or reduce the degree of pain.

• This medication is only part of the therapy for angina. The patient should try to avoid things that cause pain (stress, heavy exercise, overeating, and smoking), reduce calorie intake if weight loss is desirable, and develop a program of regular and sensible exercise.

• The patient should not eat large amounts of foods that stimulate the heart (e.g., coffee, tea, caffeinated soft drinks, chocolate).

• This medication must be kept out of the reach of children and others for whom it is not prescribed.

• In the hospital, the patient’s blood pressure should be taken before giving sublingual nitroglycerin and also between doses. Nitroglycerin may cause hypotension. Because the coronary arteries receive their blood supply during diastole, hypotension also decreases the blood flow to the coronary arteries, thus making the blood pressure even lower if the patient is having an MI. In the hospital, the nurse should remove any nitroglycerin (NTG) patches before performing cardioversion or defibrillating a patient.

Antidysrhythmics

Overview image

A person with heart disease or other diseases, or nutritional or congenital problems that may affect heart muscle, is at risk of developing irregular beating of the heart, or cardiac dysrhythmia. Because the term dysrhythmia (irregular rhythm) explains what happens to the patient better than the older term arrhythmia (without rhythm), it is now commonly used. Dysrhythmias may be fast or slow, with an irregular or regular pattern. The most common causes of dysrhythmias are irritation to the heart tissue after the patient has suffered an MI, fluid and electrolyte imbalances, problems with diet, hypoxia (reduced blood oxygen), and reactions to drugs.

The middle layer of the heart wall, or myocardium, is made up of special muscle cells. These muscle cells work together under the direction of a special group of nerve fibers called the pacemaker, which located in the sinoatrial (SA) node. The pacemaker cells direct the rest of the cardiac cells by sending electrical impulses through a special nerve system known as the cardiac conduction system. These impulses cause atrial and ventricular contraction (pumping). A person’s heart rate is governed by how fast the pacemaker cells direct the heart to pump and by how fast this information is spread through the heart. The usual path of information flow begins in the SA node, passes through the atrium to the atrioventricular (AV) node, through the bundle of His, through the right and left bundle branches, and out through the Purkinje fibers of the myocardium. When the electrical impulse has spread along this pathway, the heart will contract, forcing blood out into the arteries. After a brief rest, the cycle will begin again. This is called normal sinus rhythm.

The electrical message directing the heart to contract depends on a special balance of electrolytes (such as calcium and sodium) in the cardiac tissues and on good function of the cardiac conduction system. This electrical message is what is recorded on the electrocardiogram (ECG). Figure 15-5 illustrates the conduction system of the heart and the ECG pattern that it makes.

When the cells in the conduction system do not have enough oxygen or are destroyed or damaged through disease, or when the electrolytes are not present in the right balance, irregular heart action is found. Some patients may describe very slow, regular or irregular heartbeats; some patients may have fast, irregular heartbeats. Some individuals may only feel a little dizzy or report that their heart has “skipped a beat.” Sometimes patients have no symptoms; sometimes the symptoms are life threatening. The nurse may feel an irregular pulse or hear the irregularity with the stethoscope. The exact type of irregular rhythm can only be determined by taking an ECG. The dysrhythmia is often classified by its location and type of rhythm abnormality produced, for example, atrial tachycardia. Outside the hospital, some patients may wear a heart monitor strapped to their chest, or inside the hospital, they may be placed in a coronary care unit so they may be closely watched. The goal of any treatment plan or therapeutic regimen is for the patient’s heart to regain a normal rate and rhythm.

Research has confirmed that some individuals have a gene that places them at risk for sudden death. The problem occurs when there is lengthening or prolongation of the QT interval measured by the ECG. The problem is known as Long QT (LQT) Syndrome and is a disorder of cardiac repolarization caused by alterations in the transmembrane potassium and sodium currents. Congenital LQT is a disease of transmembrane ion-channel proteins. Six different genes might cause this problem and many members of a family may have the same problem. Single cases of the disease occur as a result of spontaneous gene mutations. The acquired causes of LQT include drugs, electrolyte imbalance, marked bradycardia, cocaine, organophosphorus compounds, subarachnoid hemorrhage, myocardial ischemia, protein sparing fasting, autonomic neuropathy, and human immunodeficiency virus disease. There are a great many drugs which might provoke this problem in at risk patients, including many cardiac and central nervous system (CNS) drugs. A complete list of drugs which these patients should not be prescribed may be found at www.sads.org/living-with-sads/Drugs-to-Avoid. When studying about drugs or reading package inserts, the nurse should be aware that some products are found to prolong the QT interval. These individuals often require internal defibrillators to be inserted into their heart.

Action image

Many dysrhythmias require placing of a pacemaker, administration of an electric shock, or other nonpharmacologic therapy. But medications do play a role. Medications that act to make the heart rhythm normal are called antidysrhythmic medications. They act on the individual cells of the heart. Each individual heart cell might be thought of as a gun. With each heartbeat, the cardiac muscle cell (gun) has to get ready to shoot (fire), fire, and then reload. As one cell discharges (fires), it triggers the next cell to discharge. After passing the electrical message to the next cell, each conduction cell must rest (reload) before it can pass another electrical signal. Antidysrhythmic drugs affect the cells that are beating (firing) irregularly by acting on each of these phases of cell activity. Dysrhythmic medications are classified by the stage at which they affect the cellular action potential. These include:

• Class I drugs (quinidine, procainamide, disopyramide):

• These drugs are sodium channel blockers. They lengthen the effective refractory period (the time period during which the cells cannot release or discharge their electrical activity [slow the reloading of the cell]) of atrial and ventricular myocardium (heart muscle) by slowing the fast inward current caused by the sodium electrolyte.

• Make the heart less excitable. Overall, the result is to slow the rate of the impulse conduction through the heart.

• Class II drugs are beta blockers, such as propranolol, esmolol, and acebutolol, which reduce sympathetic excitation to the heart (affect the loading of the cell).

• Class III drugs are potassium channel blockers (such as amiodarone) that lengthen the action potential duration, or the length of time it takes for one cell to fire and recover (slow the firing).

• Class IV drugs are calcium channel blockers (such as verapamil) that selectively block the ability of calcium to enter the myocardium and prolong the effective refractory period (or resting period) in the AV node (affect the reloading of the cell).

• There is also a miscellaneous antidysrhythmic drug category that includes digitalis and other well-known and effective drugs.

Uses

The cause of the dysrhythmia will determine which drug will be most effective in correcting it. The two basic actions within the heart that cause dysrhythmias are: (1) increased sensitivity of electrical cells in the heart, resulting in irregular or early ectopic beats (the cell fires before it should); and (2) electrical activity moving through abnormal conduction pathways (the trigger that causes the cell to fire does not always work properly). For example, a block of the sinus or AV node pacemakers force the heart to use a different pathway than usual. The amount of medication that can be given for these dysrhythmic drugs has a very small range. If too much is given, the dose may be toxic and add to the problems of the heart.

There are now many dysrhythmic drugs on the market. Only a few of the most commonly used drugs are described here. Two drugs that are often used to treat rapid and irregular dysrhythmias are quinidine and procainamide. These drugs are chemically different, but both act to quiet the myocardial cells and make them less excitable and less likely to fire. This not only decreases the heart rate but also stops some of the extra or irregular beats. These drugs were once the mainstay of dysrhythmia therapy but new drugs now have less significant side effects.

Bretylium is another drug that used to be in greater use to slow the conduction rate of the electrical impulse in the ventricular muscle. This drug also acts to slow the release of norepinephrine, a powerful chemical in the cardiac cells, so the heart muscle beats more slowly.

Disopyramide slows the depolarization of the cardiac cells. Depolarization is the movement of electrolytes into and out of the cell as it gets ready to send another electrical message. Under the influence of disopyramide, the heart rate is slowed because each cell is slower in recovering from sending the message to the next cell (the reloading time takes longer).

Lidocaine IV is a drug that was formerly widely used. The electrical impulse sent to the cardiac muscle must be of certain strength, or it cannot pass along the conducting nerve fibers. Lidocaine increases the strength of the impulse. A drug that affects the rate of rhythmic movements, such as the heartbeat, is called a chronotropic drug. A dromotropic drug influences the velocity (speed) of the passage of an electrical impulse in nerve or cardiac muscle fibers.

A diseased heart may have many electrical impulses trying to move at the same time, but some impulses are very weak. By increasing the strength the impulse must reach before it may be conducted, many weak impulses will be screened out, and the overall heart rate will be slower.

Adenosine is a powerful drug that slows the conduction through the AV node and decreases how rapidly the SA node will fire. An IV injection to end serious atrial tachycardia may cause the heart to stop beating for several seconds when a very rapid heartbeat is changed to normal (normal sinus rhythm). Although this drug has only a 10-second half-life, this pause in the heart beat is very upsetting for patients, who often refuse to take it more than once. Some institutions may use benzodiazepines at the same time to help the patients relax during this procedure.

Digoxin is used primarily to treat heart failure but also plays a role in treating fast dysrhythmias such as atrial fibrillation or tachycardia. It slows the heart rate by slowing how fast the SA node fires and slowing conduction through the AV node. It also strengthens the contraction of the heart. Toxic levels of this medication also cause dysrhythmias. (See cardiotonics in a later section.) Other drugs that affect heart activity are the beta-adrenergic blockers, of which propranolol (Inderal) and metoprolol (Lopressor) are the most well known. Drugs in this category act very much like quinidine, but they also decrease the response of the heart muscle to epinephrine and norepinephrine (other chemical neurotransmitters) by blocking the stimulation of the heart’s beta receptors. (Again, the reloading of the cell is affected.)

It is clear that many of the antidysrhythmic drugs are so powerful that they should only be used in critical care units where the patient may be closely monitored. Some of these drugs are given as an IV injection followed by an IV solution filled with the medication. As the patient’s condition becomes more stable, some drugs may be changed to other antidysrhythmic drugs that are better for long-term therapy.

Table 15-3 lists drugs that may commonly be used in the treatment of acute and chronic dysrhythmias.

image Table 15-3

Acute Treatment and Chronic Prophylaxis of Dysrhythmias

DYSRHYTHMIA TYPE OF TREATMENT INDICATED*
ACUTE CHRONIC PROPHYLAXIS
Sinus tachycardia (rarely treated) propranolol image propranolol image
Premature atrial contractions (usually in patients with history of atrial fibrillation) digoxin image digoxin image, quinidine, disopyramide, procainamide, propranolol image
Premature ventricular contractions (multifocal, on vulnerable part of T wave, or in symptomatic patient) Lidocaine image procainamide quinidine, disopyramide, procainamide, digoxin image, propranolol image
Atrial flutter/atrial fibrillation Cardioversion: digoxin image digoxin image, propranolol quinidine, disopyramide, procainamide, verapamil image
Paroxysmal supraventricular tachycardia Carotid massage; cardioversion: propranolol image, digoxin image, verapamil image, adenosine propranolol image, digoxin image, quinidine, disopyramide, procainamide, verapamil image

Image

image Indicates “Must-Know Drugs,” or the 35 drugs most prescribers use.

*Listed in order of suggested use.

Adverse Reactions

Most drugs given to control dysrhythmias may also cause other dysrhythmias. All patients receiving these drugs should have their heart carefully monitored by ECG for any change.

Quinidine is an older drug that is still in use in some hospitals and parts of the world, although it has many adverse effects. It may cause cardiac dysrhy­thmias, hypotension, diarrhea, tinnitus, headache, vertigo, confusion, delirium, disturbances in vision, and abdominal pain. Toxic effects are called cinchonism, and the patient will complain of tinnitus, light-headedness, headache, fever, vertigo, nausea, vomiting, and dizziness. The first time the patient takes the medicine, a test dose should be given to check for quinidine syncope—a condition in which the body reacts to quinidine by reducing blood flow to the brain, producing syncope (light-headedness and fainting), loss of consciousness, and sometimes death.

See Table 15-3 for common adverse effects.

Drug Interactions

Quinidine’s effect is increased by potassium and is reduced by hypokalemia. Verapamil actions are stronger when used at the same time as digitalis and beta blockers. Beta blockers have many interactions with other drugs, and the nurse should read about every other drug the patient is taking when a beta blocker is prescribed.

imageNursing Implications and Patient Teaching

n Assessment

Learn everything possible about the patient’s health history, including any drug allergies, other drugs being taken that may cause drug interactions, and other medical problems, including factors such as hypoxia (reduced blood oxygen), acid-base imbalance, increased or decreased potassium, or drug toxicity. It is good practice to always take an apical heart rate with any patient that may have an arrhythmia by placing the stethoscope in the left chest cardiac area. Some irregular heart rates are very weak and are difficult to accurately feel with a radial pulse.

n Diagnosis

Does the patient have other health problems that will affect therapy? Does the patient drink lots of caffeine? Smoke? Exercise? Is the patient overweight?

n Planning

An ECG should be obtained before medications are started. This will determine the status of the heart before treatment so that changes can be seen if treatment is helpful.

n Implementation

Vital signs must be taken before giving any antidysrhythmic medication. The nurse often has the responsibility of monitoring any changes that might develop in blood pressure or pulse while initial thrapy is given. Hospitalized patients often continue their antidysrhythmic medications when they go home, so the nurse might take advantage of every opportunity to teach patients about these medications and be prepared to answer questions.

Table 15-4 presents information about the antidysrhythmics.

image Table 15-4

Antidysrhythmics

GENERIC NAME TRADE NAME USES ADVERSE REACTIONS
Class I Drugs
A
disopyramide Norpace, Napamide Treat ectopic ventricular dysrhythmias Constipation, urinary hesitancy, headache, dry mouth, blurred vision, nausea dizziness, headache, and fatigue
procainamide Procanbid
Pronestyl
Pronestyl SR
PVCs, ventricular tachycardia, atrial fibrillation, and PAT Anorexia (lack of appetite), rash, pruritus, nausea, severe hypotension, and ventricular dysrhythmias
quinidine (sulfate or gluconate or polygalacturonate) Duraquin
Quinaglute, Quinidex
PACs, PVCs, PAT, atrial flutter, and atrial fibrillation Tinnitus, disturbed vision, headache, nausea, and dizziness
B
lidocaine image (without preservatives) Xylocaine Life-threatening ventricular dysrhythmias Bradycardia, drowsiness, hypotension, light-headedness, convulsions tinnitus (ringing in the ears), blurred or double vision, bradycardia (slow heartbeat), and hallucinations
mexiletine Mexitil Symptomatic ventricular dysrhythmias GI distress, tremor, light-headedness, incoordination, and hepatic and hematologic effects
Phenytoin Dilantin Unlabeled use for dysrhythmias  
Tocanide Tonocard Usually reserved for serious ventricular arrhythmias  
C
flecainide Tambocor Usually reserved for serious ventricular dysrhythmias  
propafenone Rythmol
Rythmol SR
Life-threatening ventricular dysrhythmias Dizziness, unusual taste, AV block, nausea, and vomiting
D
moricizine (does not belong to A, B, or C category, but shares some characteristics of each) Ethmozine Severe ventricular dysrhythmias May provoke other dysrhythmias.
Class II Drugs: Beta Blockers (see section on antihypertensives)
acebutolol Sectral Ventricular tachycardia Bradycardia and dizziness
esmolol Brevibloc Supraventricular tachycardia Bradycardia and dizziness
propranolol image Inderal
Pronol
Cardiac dysrhythmias, migraine, angina, MI, and pheochromocytoma Bradycardia, dizziness, vertigo, rash, bronchospasm, hyperglycemia, hypertension, visual disturbances, fatigue, chest pain, arthralgia (joint pain), and pruritus
Class III Drugs
amiodarone Cordarone
Pacerone
Life-threatening ventricular dysrhythmias GI distress, CNS symptoms, and photosensitivity (abnormal response to exposure to sunlight); pulmonary fibrosis
bretylium Bretylol Usually reserved for life-threatening ventricular dysrhythmias; IM form available  
dofetilide Tikosyn Used to convert atrial fibrillation/atrial flutter and maintain normal sinus rhythm May precipitate other fatal dysrhythmias.
ibutilide Corvert atrial fibrillation or flutter  
sotalol Betapace
Sorine
Life-threatening ventricular tachycardia Life-threatening ventricular tachycardia
Class IV Drugs Calcium Channel Blockers
verapamil image Calan
Isoptin
Verelan
Isoptin SR
Supraventricular tachydysrhythmias Cardiac dysrhythmias, CHF, and hypotension
It forms a cloudy mixture that cannot be injected if it is mixed in the same syringe or bottle with sodium bicarbonate or nafcillin.
Miscellaneous Drugs for Dysrhythmias
adenosine Adenocard Supraventricular tachycardia Facial flushing and shortness of breath
Digoxin Lanoxin Used primarily in atrial dysrhythmias.  

Image

AV, Atrioventricular; CHF, congestive heart failure; CNS, central nervous system; GI, gastrointestinal; IM, intramuscular; MI, myocardial infarction; PAC, premature atrial contraction; PAT, paroxysmal atrial tachycardia; PVC, premature ventricular contraction.
image Indicates “Must-Know Drugs,” or the 35 drugs most prescribers use.

n Evaluation

If the patient’s heart is not being watched with a cardiac monitor, the results from ECGs must be closely followed to see any changes. Electrolyte levels and other laboratory data should also be obtained.

n Patient and Family Teaching

Tell the patient and family the following:

Antihyperlipidemics

Overview

Cholesterol and other fatty acids are called lipids. The body needs a certain amount of cholesterol and triglycerides, which are both normal and vital parts of blood plasma. Like other lipids, they are not soluble in liquid, so they are carried in the plasma by linking to lipo­proteins (albumin and globulins). Lipoproteins are described by how thick or dense they are (“high-density lipids” and “low-density lipids”). The four major types of lipoproteins are as follows:

1. Chylomicrons. These are the largest and lightest of the lipoproteins. They are formed from the absorption of dietary fat in the intestine and are mostly triglycerides. Chylomicrons are normally present in plasma for only 1 to 8 hours after the last meal, and they make the plasma look cloudy. If a tube of blood from a fasting patient shows a thick layer of fat or cloudy plasma after several hours, the patient may have an inability to handle dietary fat.

2. Very-low-density lipoproteins (VLDLs). These are made up of large amounts of triglycerides that were made in the liver and are called pre-beta lipoproteins. The pre-beta form is a carrier state for moving triglycerides that have been produced in the liver into the plasma. Nearly all the triglycerides in plasma that are not in chylomicrons are considered to be VLDLs.

3. Low-density lipoproteins (LDLs). When VLDLs break down and link with cholesterol and protein, very little triglyceride is left. What remains is then called beta lipoprotein. Approximately 75% of the cholesterol in plasma is moved in this form. High serum levels of LDLs indicate cholesterol levels that are higher than the body needs. Patients with high LDL levels are at high risk for developing atherosclerosis.

4. High-density lipoproteins (HDLs). These small, dense lipoproteins are called alpha lipoproteins and contain very small parts of triglycerides. They are mostly made up of protein and cholesterol. They serve as the “vacuum cleaners” of the tissues, clearing out excess cholesterol. They may prevent atherosclerotic activity by blocking uptake of LDL cholesterol by vascular smooth muscle cells.

Chylomicrons and VLDLs are seen as triglyceride-rich lipoproteins, whereas LDLs and HDLs are viewed as cholesterol-rich lipoproteins. These two lipoproteins differ in several respects, including their cholesterol transporting activities. Simply stated, LDLs move cholesterol from the liver to peripheral tissues, and HDLs remove cholesterol from the periphery and transport it to the liver. Figure 15-6 shows the normal physiology of lipoprotein transport. Chylomicrons are the largest and least dense of the lipoproteins; as size decreases and density increases, the next type is the VLDLs (pre-beta lipoproteins), then the intermediate-density lipoproteins (IDLs, or broad beta lipoproteins), then the LDLs (beta lipoproteins), and finally the HDLs (alpha lipoproteins, the smallest and most dense).

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